Cardiovascular disease is a major disease that threatens human life and health. As society progresses and people's living standards improve, its incidence increases year by year. In 2014, the number of deaths resulted from cardiovascular disease accounted for about 30% of the total global death toll, and myocardial ischemic disease is the focus of cardiovascular disease and can develop into arrhythmia, myocardial infarction, and often life-threatening. Therefore, how to practically and effectively reduce the damage caused by myocardial ischemia has become a hot topic in the medical field.
Myocardial ischemic damage is the result of myocardial cell necrosis or impaired function caused by cardiomyocyte hypoxia. The most commonly used drugs in the clinic nowadays are to treat myocardial ischemia by improving cellular energy metabolism, inhibiting inflammatory response, protecting blood vessels, and alleviating calcium overload in cardiomyocytes and the most commonly used drugs include nitrates such as nitroglycerin, isosorbide dinitrate; beta-blockers such as propranolol; calcium channel blockers such as nifedipine and verapamil as well as antiplatelet and antithrombotic drugs such as dipyridamole.
Neuraminidase (NA) is a glycoprotein on the surface of influenza virus with exoglycosidase activity that cleaves α-glycosidic bonds between cell surface sialic acid and adjacent lactose. During the entire life cycle of influenza virus, NA plays a role in recognizing receptors for influenza virus-infected cells and promoting virus' entry into recipient cells. This process plays a key role in viral infection and transmission. Therefore, neuraminidase is an important target for the development of anti-influenza drugs. The currently used neuraminidase inhibitors, zanamivir and oseltamivir phosphate, play an important role in the prevention and treatment of influenza.